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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In pharmacological doses dopamine (DA) will interact with several endocrine systems and both inhibit (prolactin, thyrotropin) and enhance (renin, angiotensin) hormonal release. In this study we have examined whether DA given to preterm neonates will influence prostaglandin (PG) production. The question is of importance since vasodilator PGs play a role in postnatal adaptation. We determined the effect of low dose DA infusion on the 24 h urinary PGE2 excretion rate (an index of renal PGE2 synthesis) in preterm infants. Six preterm neonates, with a 24-h requirement of 2 micrograms/kg per min DA treatment for oedema, moderate oliguria, poor peripheral perfusion and/or mild systemic hypotension were studied on days 2 (Day 1), 3 (Day 2, the day of DA infusion), and 4 (Day 3, DA discontinued) of life. Six preterm infants (control group) that did not require DA infusion were also studied to monitor possible spontaneous changes in the renal PGE2 production on days 2, 3 and 4 of life. In the control group urine output (Uv) and PGE2 excretion rate remained unchanged during the study. In the study group DA administration resulted in nearly two-fold increases in both the Uv (194%) and PGE2 excretion (182%). Urinary PGE2 excretion was, however, closely related to urine flow in both the control infants (Day 1-3) and the study group infants (Day 1-2). Since increased diuresis stimulates renal PGE2 production, our data suggest that the increased PGE2 excretion on Day 2 in the study group was not due to a direct effect of DA on PGE2 synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of low-dose dopamine infusion on urinary prostaglandin E2 excretion in sick, preterm infants. 318 Dec 3

A retrospective study of nine sick premature infants with chronic lung disease who received captopril for control of systemic hypertension (systolic blood pressure (BP) greater than 113 mm Hg) was carried out to determine efficacy of therapy and associated complications. All nine infants had markedly elevated peripheral renin values, 134.3 +/- 128.1 ng/mL/hr (mean +/- SD). Five infants had abnormal renal sonographic and perfusion scans with evidence of renal artery thrombosis, parenchymal disease, or both. Captopril therapy (0.3 mg/kg) was instituted at a postnatal age of 123 +/- 108 days. After the initial dose, the systolic BP decreased significantly in all infants, the decrease ranging from 21% to 58% of the pretreatment value. Dosage was subsequently halved in all infants. Seventeen episodes of unpredictable decreases in BP more than 40% from baseline occurred during the reduced maintenance therapy. Four infants had a total of seven episodes during which the BP decreased by 57 +/- 10% from baseline; this decrease persisted for 17 +/- 6 hours and was unresponsive to volume reexpansion and inotropic therapy. All seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/hr) that persisted for 18 +/- 12 hours. These episodes were accompanied by neurologic signs (subtle seizures, lethargy, and/or apnea) within 18 +/- 6 hours after the onset of oliguria. The remaining five infants had a total of 13 episodes of decreased BP of 50 +/- 8% of baseline, which were of significantly shorter duration and responded to volume reexpanders, inotropic therapy, or both and were unaccompanied by oliguria. These data suggest the need for close observation of BP in infants receiving maintenance captopril therapy.
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PMID:Renal failure in sick hypertensive premature infants receiving captopril therapy. 328 14

Acute oliguria in the critically ill postoperative patient, or in the trauma victim after resuscitation, is a substantial clinical problem. The mortality associated with ARF in these settings remains unacceptably high. Evaluation of the oliguric patient must include thorough monitoring for, and correction of, prerenal and postrenal causes of oliguria. In this sense, diagnosis of ARF is one of exclusion. Differential diagnosis is facilitated by microscopic examination of urine and by biochemical analyses of blood and urine for calculating indices of tubular function (urinary-to-plasma ratios of blood urea nitrogen and creatinine, sodium excretion, and clearances of sodium, creatinine, solute, and water). The early detection of an intrarenal defect, as accomplished by using serial measurements of free water clearance, may allow interruption of the process and prevention of ARF. Preventive measures include optimization of hemodynamic status and the use of osmotic diuretic agents (mannitol) and loop diuretics (furosemide, ethacrynic acid, and bumetanide). Dopamine is useful for increasing both renal blood flow and urine flow and may be useful for preventing ARF, but this is not firmly established. Experimentally, other approaches such as modulating the renin-angiotensin system, prostaglandin system, and cellular calcium fluxes have been attempted, but the clinical applicability of these measures is not established. The best approach to ARF is preventing it by knowing which patients are at high risk, by studiously preventing renal insults, and by aggressively treating early indications of renal malfunction using established therapies.
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PMID:Acute renal failure following traumatic injury or major operation. 355 12

We describe an animal model of generalized sepsis, induced in the sheep by cecal perforation, which reproduces the high systemic flow and peripheral vasodilation seen in early human sepsis. Despite volume loading, animals demonstrate a fall in glomerular filtration rate, oliguria, low fractional sodium excretion, maintained urine osmolarity, and increased plasma renin activity. Histologically, kidneys show no consistent abnormality; overall the findings suggest volume contraction or hypoperfusion. This is contradicted, however, by maintained blood pressure and pulmonary capillary wedge pressure, increased cardiac output, and reduced peripheral resistance. Increased Fc lysozyme and low molecular weight proteinuria suggest tubular damage. These paradoxical observations are currently unexplained.
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PMID:The renal response produced by nonhypotensive sepsis in a large animal model. 374 63

1. Rats in normal fluid balance drank water 1-2 hr after complete ligation of the inferior vena cava either above or below the renal veins. At the same time there was a fall in urine flow and excretion of electrolyte, especially after caval ligation above the renal veins, so that the animals ended the initial 6 hr period in positive fluid balance.2. Caval ligation was relatively ineffective as a stimulus to drinking after bilateral nephrectomy, but was effective in rats made anuric by ureteric ligation.3. Rats subjected to caval ligation and offered a choice between water and 1.8% saline (w/v) drank water, despite the increasing hypotonicity of the body fluids thereby resulting.4. During the secondary polydipsia, which generally occurred on about the third day after caval ligation as renal function was recovering, there was an increased preference for 1.8% saline.5. Constriction of the aorta above the renal arteries, or constriction of both renal arteries, also caused drinking, oliguria and the development of positive fluid balance.6. Constriction of the aorta below the renal arteries, or after nephrectomy, was ineffective as a stimulus to drinking.7. Saline extracts of renal cortex caused rats in normal water balance to drink. Activity was destroyed by boiling the extract for 10 min. Renal medullary and hepatic extracts were without effect on drinking.8. It proved impossible to separate dipsogenic and pressor activities of renal extracts during the different stages of fractionation which lead to the production of renin; disappearance of one activity was invariably accompanied by disappearance of the other.9. Dipsogenic and pressor actions were greater in nephrectomized rats than in normal rats.10. Both extractable dipsogenic factor and extractable pressor activity were reduced by treating the rat with DOCA and saline for several weeks beforehand.11. The renal dipsogen therefore has similar properties to renin. It may prove to be identical with renin, particularly in view of the fact that angiotensin also stimulates drinking.12. Adrenalectomy did not affect drinking induced by renin or by caval ligation.13. It is concluded that the renin angiotensin system may play a role in the genesis of the thirst which follows certain extracellular stimuli.
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PMID:The role of a renal thirst factor in drinking induced by extracellular stimuli. 430 8

A strong inverse relationship was found between the excretion rates of the prostaglandins PGE2 and PGF2 alpha and urine flow (and osmolar excretion rate) over a range of urine flow rates from 1.5 to 40 microliters . min-1 . g kidney weight-1, covering spontaneous variations and isotonic saline diuresis. These results suggest the operation of a negative feedback mechanism by which the diuretic action of the prostaglandins, as part of a defence system, counteracts excessive oliguria. PGE2 excretion did not correlate with either urinary kallikrein excretion or plasma renin concentration. When the concentrating mechanism was interfered with by reducing renal perfusion pressure to, or below 65 mmHg, and vasopressin was given i.v. PGE2 excretion rate roughly parallelled urine--and probably medullary interstitial osmolar activity. However, in hydropenic rats there was no correlation between urine osmolality (Uosm) and PGE2 excretion over a range of osmolalities from 500 to 2 500 mOsm . kg-1, nor any relationship between delta Uosm and delta PGE2 excretion. Thus, a high interstitial osmolar activity appears to be a prerequisite for the activation of PG-synthesis in the renal medulla, but another (other) yet undefined factor(s) play the major role as (a) determinant(s) for PG-excretion in vivo.
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PMID:On the relationship between urinary PGE2 and PGF2 alpha excretion rates and urine flow, osmolar excretion rate and urinary osmolality in anesthetized rats. 695 76

Eight hypertensive children with acute post-streptococcal glomerulonephritis were given intravenous frusemide, 2 mg/kg, and the results compared with 8 similar cases not given the diuretic. Mean urine flow increased from 0.24 ml/min/m2 before frusemide to 3.63 ml/min/m2 in the 6 hours afterwards and was still 0.72 ml/min/m2 48 hours later. In contrast mean urine flow remained unchanged over 48 hours in those not given frusemide. Despite similar initial blood pressures the duration of hypertension was much shorter (mean 4.7 days) after frusemide than in the controls (mean 11.0 days) and the edema-free weight was achieved more rapidly (6.8 days compared with 13.9 days). Plasma renin activity (PRA) did not rise after frusemide in the children with acute nephritis. This was in contrast to the rapid rise seen in normal humans thus indicating a dissociation between the diuretic and renin-releasing activities of frusemide in acute nephritis. Seven children with the hemolytic-uremic syndrome or acute tubular necrosis showed no significant change in either urine flow or PRA after frusemide. Frusemide is therefore effective treatment for both hypertension and oliguria in acute nephritis. Failure of PRA to rise indicates that renin release mechanisms are abnormal in renal failure and that PRA levels need to be interpreted with caution in this condition.
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PMID:Response to frusemide in acute renal failure: dissociation of renin and diuretic responses. 699 79

Hemodynamic and renal function response to low-dose (100 and 200 micrograms/min) dopamine infusion was studied in 15 adult cardiac surgical patients who manifested combined oliguria and left ventricular dysfunction postoperatively. Patients were studied an average of 6.6 h after ICU admission, at normothermia and after 2 consecutive hourly urine output determinations of less than 0.5 ml/kg . h in the presence of a left atrial or pulmonary artery occlusion pressure over 12 mm Hg. Dopamine infusion at 100 micrograms/min produced improvement in creatinine, osmolar and free water clearances (70 +/- 10 to 115 +/- 13, 37 +/- 4 to 93 +/- 16 and --15 +/- 2 to --37 +/- 10 ml/min, respectively), and urinary sodium concentration (15 +/- 5 to 29 +/- 10 mEq/L). Urine flow improved overall from 22 +/- 2 to 54 +/- 9 ml/h; however, in 9 of 15 patients, flow was less than 0.5 ml/kg . h (33 +/- 5 to 50 +/- 6 ml/h). In each of these 9 patients, dopamine infusion at 20 micrograms/min further improved urine flow as well as measured renal function. Plasma renin activity measured in 9 of the 15 patients before and during the 100 micrograms/min dopamine infusion was decreased from 1.95 +/- 0.57 to 0.73 +/- 0.39 ng/ml . h. The hemodynamic effect of both dopamine doses was increased cardiac output coupled with decreased systemic (SVRI) and pulmonary vascular resistance index (PVRI). In these 15 patients, low-dose dopamine infusion produced significant improvement in renal function, with resolution of oliguria in every case, and with no deleterious hemodynamic effect.
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PMID:Acute oliguria after cardiopulmonary bypass: renal functional improvement with low-dose dopamine infusion. 714 Mar 33

The hepato-renal syndrome is defined as potentially reversible functional renal failure associated with acute fulminant hepatitis or, more often, with advanced chronic liver failure. It is characterized by oliguria, azotemia, retention of sodium and water with formation of ascites, and hyponatremia. While urinary sodium concentration of less than 10 mEq/l reflects intact tubular sodium absorption, the kidney lacks the ability for adequate free-water generation. This condition must be separated from specific renal diseases which may arise during the course of intra-or extrahepatic diseases and which must be classified accordingly. Pathophysiological aspects of the hepa-to-renal syndrome include hemodynamic factors, such as changes in intrarenal blood flow distribution in the presence of elevated intrarenal and reduced peripheral vascular resistance. The functional relationship of vasoconstrictor, sodium retaining, and anti-diuretic hormones (e.g., renin-angiotensin, aldosterone, and vasopressin) to vasodilator, diuretic, and natriuretic hormonal factors (e.g., prostaglandins, kinins, and natriuretic hormone) may be altered as well. Finally, a pre- and intrahepatic spillover resulting in decreased endotoxin clearance must be considered. Due to the lack of understanding of their complex interactions, so far pharmacological and therapeutic approaches remained ineffective to correct at least some of these factors. Today, recovery from hepato-renal syndrome will, therefore, mainly depend on the course of the underlying liver disease.
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PMID:[Hepato-renal syndrome (author's transl)]. 727 84

Thorough studies of kidney specimens obtained at autopsy or by renal biopsy revealed, that in noninflammatory acute renal failure oliguria/anuria is caused by increased activation o the renal renin-angiotensin system and increased generation of adenosine. At the polyuric phase moderately increased adenosine in kidney tissue seems to be the main factor responsible for decreased glomerular filtration.
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PMID:[Acute noninflammatory renal failure. New pathogenetic aspects in light of findings obtained in autopsy and biopsy of kidneys]. 793 95


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